Low involvement of preexisting associations makes retrieval-induced forgetting long lasting.

Research has shown that selective retrieval of episodic memories usually leads to forgetting of related memories that compete for retrieval [a phenomenon known as retrieval-induced forgetting (RIF)]. However, there are conflicting data regarding the duration of this incidental kind of forgetting. While some studies have found that this forgetting effect disappears within 24 h after selective retrieval, others suggest that it may last for as long as at least a week. In two experiments, we explored whether discrepancies in the durability of RIF may be due to variations in the type of relationships (preexisting vs. novel) that are present between items associated with a given cue. We explored this issue by manipulating the degree of involvement of preexisting/novel associations among competing items as well as the delay between retrieval practice and test (immediate in Experiment 1 and 24-h delay test in Experiment 2). The results suggest that forgetting lasts longer when the degree of preexisting associations among targets and competitors is low.

p38 MAPK protects human monocytes from postprandial triglyceride-rich lipoprotein-induced toxicity.

Postprandial triglyceride (TG)-rich lipoproteins (TRLs) transport dietary fatty acids through the circulatory system to satisfy the energy and structural needs of the tissues. However, fatty acids are also able to modulate gene expression and/or induce cell death. We investigated the underlying mechanism by which postprandial TRLs of different fatty acid compositions can induce cell death in human monocytes. Three types of dietary fat [refined olive oil (ROO), high-palmitic sunflower oil (HPSO), and butter] with progressively increasing SFA:MUFA ratios (0.18, 0.41, and 2.08, respectively) were used as a source of postprandial TRLs (TRL-ROO, TRL-HPSO, and TRL-BUTTER) from healthy men. The monocytic cell line THP-1 was used as a model for this study. We demonstrated that postprandial TRLs increased intracellular lipid accumulation (31-106%), reactive oxygen species production (268-349%), DNA damage (133-1467%), poly(ADP-ribose) polymerase 1 (800-1710%) and caspase-3 (696-1244%) activities, and phosphorylation of c-Jun NH2-terminal kinase (JNK) (54 kDa, 141-288%) and p38 (24-92%). These effects were significantly greater with TRL-BUTTER, and TRL-ROO did not induce DNA damage, DNA fragmentation, or p38 phosphorylation. In addition, blockade of p38, but not of JNK, significantly decreased intracellular lipid accumulation and increased cell death in postprandial TRL-treated cells. These results suggest that in human monocytes, p38 is involved in survival signaling pathways that protect against the lipid-mediated cytotoxicity induced by postprandial TRLs that are abundant in saturated fatty acids.

Triglyceride-rich lipoprotein regulates APOB48 receptor gene expression in human THP-1 monocytes and macrophages.

The postprandial metabolism of dietary fats implies that the production of TG-rich lipoproteins (TRL) contributes to the progression of plaque development. TRL and their remnants cause rapid receptor-mediated monocyte/macrophage lipid engorgement via the cell surface apoB48 receptor (apoB48R). However, the mechanistic basis for apoB48 receptor (APOB48R) regulation by postprandial TRL in monocytes and macrophages is not well established. In this study, we investigated the effects of postprandial TRL from healthy volunteers on the expression of APOB48R mRNA and lipid uptake in human THP-1 monocytes and THP-1-derived macrophages. The expression of APOB48R mRNA was upregulated in THP-1 monocytes, but downregulated in THP-1-derived macrophages when treated with postprandial TRL (P < 0.05), in a dose- and time-dependent manner. TG and free cholesterol were dramatically increased in THP-1-derived macrophages (140 and 50%, respectively; P < 0.05) and in THP-1 monocytes (160 and 95%, respectively; P < 0.05). This lipid accumulation was severely decreased (~50%; P < 0.05) in THP-1-derived macrophages by small interfering RNA (siRNA) targeting of APOB48R. Using PPAR and retinoid X receptor (RXR) agonists, antagonists, and siRNA, our data indicate that PPARα, PPARγ, and RXRα are involved in postprandial TRL-induced APOB48R transcriptional regulation. Co-incubation with acyl-CoA synthetase or acyl-CoA:cholesterol acyltransferase inhibitors potentiated the effects of postprandial TRL on the expression of APOB48R mRNA in THP-1 monocytes and THP-1-derived macrophages. Our findings collectively suggest that APOB48R represents a molecular target of postprandial TRL via PPAR-dependent pathways in human THP-1 monocytes and macrophages and advance a potentially important link between postprandial metabolism of dietary fats and atherogenesis.

Memory inhibition, aging, and the executive deficit hypothesis.

Although memory inhibition seems to underlie retrieval-induced forgetting (RIF), there is some controversy about the precise nature of this effect. Because normal RIF is observed in people with deficits in executive control (i.e., older adults), some have proposed that an automatic-like inhibitory process is responsible for the effect. On the contrary, neurocognitive and dual-task findings with young people support the view that an executive control process underlies RIF. In the present study, we address this apparent controversy by comparing young and older participants under different dual-task conditions. Our results indicate that memory inhibition in older adults also depends on executive control, which is more easily disrupted by a secondary task in older than in young adults. Thus, the fact that RIF in older adults is sometimes present is not incompatible with a decline in executive control with aging. The results also shed some light into the discussion regarding the effect of dual tasking on retrieval.

Dietary fatty acids linking postprandial metabolic response and chronic diseases.

Chronic diseases are by far one of the main causes of mortality in the world. One of the current global recommendations to counteract disability and premature death resulting from chronic diseases is to decrease the consumption of energy-dense high-fat diets, particularly those rich in saturated fatty acids (SFA). The most effective replacement for SFA in terms of risk factor outcomes for chronic disease are polyunsaturated fatty acids (PUFA) and monounsaturated fatty acids (MUFA). The biochemical basis for healthy benefits of such a dietary pattern has been widely evaluated under fasting conditions. However, the increasing amount of data available from multiple studies suggest that the postprandial state, i.e., "the period that comprises and follows a meal", plays an important, yet underappreciated, role in the genesis of numerous pathological conditions. In this review, the potential of MUFA, PUFA, and SFA to postprandially affect selected metabolic abnormalities related to chronic diseases is discussed.

Effects of meals rich in either monounsaturated or saturated fat on lipid concentrations and on insulin secretion and action in subjects with high fasting triglyceride concentrations.

BACKGROUND: The nature of dietary fats and fasting concentrations of triglycerides affect postprandial hypertriglyceridemia and glucose homeostasis. OBJECTIVES: The objectives were to examine the effects of meals enriched in monounsaturated fatty acids (MUFAs) or saturated fatty acids (SFAs) on postprandial lipid, glucose, and insulin concentrations and to examine the extent of ß cell function and insulin sensitivity in subjects with high fasting triglyceride concentrations. DESIGN: Fourteen men with fasting hypertriglyceridemia and normal glucose tolerance were given meals (≈10 kcal/kg body weight) containing MUFAs, SFAs, or no fat. Blood samples were collected at baseline and hourly over 8 h for analysis. RESULTS: The high-fat meals significantly increased postprandial concentrations of triglycerides, nonesterified fatty acids, and insulin and postprandial indexes of ß cell function. However, postprandial indexes of insulin sensitivity decreased significantly. These effects were significantly attenuated with MUFAs relative to SFAs. CONCLUSIONS: MUFAs postprandially buffered ß cell hyperactivity and insulin intolerance relative to SFAs in subjects with high fasting triglyceride concentrations. These data suggest that, in contrast with SFAs, MUFA-based strategies may provide cardiovascular benefits to persons at risk by limiting lipid and insulin excursions and may contribute to optimal glycemic control after meal challenges.

A high-fat meal promotes lipid-load and apolipoprotein B-48 receptor transcriptional activity in circulating monocytes.

BACKGROUND: The postprandial metabolism of dietary fats results in the production of apolipoprotein B-48 (apoB48)-containing triglyceride-rich lipoproteins (TRLs), which cause rapid receptor-mediated macrophage lipid engorgement via the apoB48 cell surface receptor (apoB48R). Monocytes circulate together with apoB48-containing TRLs in the postprandial bloodstream and may start accumulating lipids even before their migration to tissues and differentiation to macrophages. OBJECTIVE: We sought to determine whether circulating monocytes are equipped with apoB48R and whether, in the postprandial state, circulating monocytes accumulate lipids and modulate apoB48R transcriptional activity after intake of a high-fat meal. DESIGN: In a crossover design, we studied the effect of a high-fat meal on fasting and postprandial concentrations of triglycerides, free fatty acids, cholesterol, and insulin in 12 healthy men. TRLs and monocytes were freshly isolated at fasting, hourly until the postprandial peak, and at the late postprandial phase. TRLs were subjected to triglycerides, apoB48, and apolipoprotein B-100 analyses; and lipid accumulation and apoB48R mRNA expression levels were measured in monocytes. RESULTS: Monocytes showed a time-dependent lipid accumulation in response to the high-fat meal, which was paralleled by an increase in apoB48R mRNA expression levels. These effects were coincident only with an increase in apoB48-containing TRLs in the postprandial phase and were also observed ex vivo in freshly isolated monocytes incubated with apoB48-containing TRLs. CONCLUSION: In a setting of abundant plasma apoB48-containing TRLs, these findings highlight the role of dietary fat in inducing lipid accumulation and apoB48R gene transcription in circulating monocytes.

Oleic acid in olive oil: from a metabolic framework toward a clinical perspective.

Traditionally, nutrients such as fatty acids have been viewed as substrates for the generation of high-energy molecules and as precursors for the biosynthesis of macromolecules. However, accumulating data from multiple lines of evidence suggest that dietary fatty acids are linked not only to health promotion but also to disease pathogenesis. Metabolism in humans is regulated by complex hormonal signals and substrate interactions. For many years, the clinical focus has centered on a wide metabolic picture after an overnight fast. Nonetheless, the postprandial state (i.e., "the period that comprises and follows a meal") is an important one, and silent disturbances in this period are involved in the genesis of numerous pathological conditions, including atherosclerosis. In this review article, we present an overview of the evidence demonstrating the relevance of oleic acid in olive oil on different nutrition-related issues. We also discuss the impact of oleic acid in olive oil and its clinical relevance to major risk factors for cardiovascular disease in the context of the postprandial state and with regard to other dietary fatty acids.

¿Perjudica Antonio Banderas a Javier Bardem?: La competición semántica en tareas de nombrado de personas / Will Antonio Banderas harm Javier Bardem?: Semantic competition during face naming

En este experimento se ha investigado la presencia de competición semántica en el nombrado de fotografías de personas conocidas. Un estudio previo de Vitkovitch, Potton, Bakogianni y Kinch (2006) mostró el efecto contrario de facilitación semántica en el nombrado de la fotografía de una persona conocida tras la recuperación, tres ensayos antes, del nombre de otra persona relacionada categorialmente. En el experimento actual se ha replicado este efecto de facilitación semántica en el nombrado de fotografías de personas relacionadas observado por Vitkovitch et al. Sin embargo, se ha observado que este efecto de facilitación semántica disminuía cuando aumentaba el número de personas nombradas de la misma categoría. Estos resultados sugieren que el nombrado de caras, de igual modo que el nombrado de objetos, está semánticamente mediado y es vulnerable a procesos de interferencia tal y como predicen los modelos de tipo serial(AU)

This experiment studies semantic competition during naming of famous faces. Previous results (Vitkovitch, Potton, Bakogianni, & Kinch, 2006) have shown semantic priming instead of semantic competition when participants were asked to name a target face after naming a categorically related priming face 3 trials before. Results of the present experiment replicated this semantic priming effect during naming. However, we also found a decrement in semantic facilitation when the number of named faces from the same category was increased. These results suggest that face naming, like object naming, is semantically mediated and vulnerable to interference processes as predicted by serial naming models(AU)